aspartic acid/infarkt

OBJECTIVE Atherosclerosis is considered to be a chronic inflammatory disease. Toll-like receptor 4 (TLR-4), a key mediator in activating inflammatory cascade, has an A-to-G functional polymorphism that changes aspartic acid to glycine at position 299. TLR-4 is activated by, for example,

Transforming growth factor-alpha attenuates N-methyl-D-aspartic acid toxicity in cortical cultures by preventing protein synthesis inhibition through an Erk1/2-dependent mechanism.

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Transforming growth factor-alpha (TGF-alpha), a ligand of the epidermal growth factor receptor, reduces the infarct size after focal cerebral ischemia in rat, but the molecular basis underlying the protection is unknown. Excitotoxicity and global inhibition of translation are acknowledged to

[Analysis of ¹H-MRS in patients with depression after basal ganglia infarction].

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OBJECTIVE To investigate the metabolic changes on proton magnetic resonance spectroscopy (¹H-MRS) in patients with first left basal ganglia infarction and their relationship with depression. METHODS Twenty-two patients with first left basal ganglia infarction and 10 matched healthy controls were

Imaging of integrin α(V)β(3) expression using (68)Ga-RGD positron emission tomography in pediatric cerebral infarct.

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Enhanced expression of integrin αvβ3 is commonly used as a biomarker for angiogenesis, which is one of the key pathophysiologic processes in cerebral infarct. Integrin αvβ3 can be imaged with arginine-glycine-aspartic acid (RGD) peptide agents. In this study, characteristics of positron emission

[Longitudinal change of H-1 spectroscopy in cerebral infarction].

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Longitudinal change of the proton spectroscopy was observed in 2 cases of cerebral infarction. Proton spectra was acquired utilizing stimulated echo acquisition mode (STEAM). In acute stage, the increase of lactic acid and decrease of N-acetyl-aspartic acid (NAA) was observed prior to the appearance

-(S)-Alpha-phenyl-2-pyridine-ethanamine Dihydrochloride-, a low affinity uncompetitive N-methyl-D-aspartic acid antagonist, is effective in rodent models of global and focal ischemia.

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[(S)-Alpha-phenyl-2-pyridine-ethanamine dihydrochloride] (ARL 15896AR) is a low affinity uncompetitive N-methyl-D-aspartic acid receptor antagonist that was tested in animal models of anoxia and ischemia. Pretreatment of rodents with ARL 15896AR extended survival time during exposure to hypoxia.

Association between the LPL-D9N mutation in the lipoprotein lipase gene and plasma lipid traits in myocardial infarction survivors from the ECTIM Study.

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Using polymerase chain reaction (PCR) based techniques, we have identified individuals in the ECTIM study of myocardial infarction survivors (cases) and healthy matched controls who are carriers for a mutation of the gene for lipoprotein lipase (LPL) which alters amino acid 9 from aspartic acid to

RGD-PEG-PLA Delivers MiR-133 to Infarct Lesions of Acute Myocardial Infarction Model Rats for Cardiac Protection

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Studies have shown that microRNA-133 (miR-133) plays a positive role in the growth of cardiac myocytes, the maintenance of cardiac homeostasis, and the recovery of cardiac function, which is of great significance for the recovery of acute myocardial infarction. However, the delivery of miRNA to the

Cellular correlates of neuronal hyperexcitability in the vicinity of photochemically induced cortical infarcts in rats in vitro.

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Intrinsic membrane properties and synaptic responses of neocortical neurons located lateral to photochemically induced ischemic lesions were investigated using neocortical slice preparation. In comparison to neurons from control slices, these neurons had a significantly less negative resting

MicroPET/CT imaging of αvβ₃ integrin via a novel ⁶⁸Ga-NOTA-RGD peptidomimetic conjugate in rat myocardial infarction.

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OBJECTIVE The αvβ3 integrin is expressed in angiogenic vessels and is a potential target for molecular imaging of evolving pathological processes. Its expression is upregulated in cancer lesions and metastases as well as in acute myocardial infarction (MI) as part of the infarct healing process. The

Preparation of high bioactivity multilayered bone-marrow mesenchymal stem cell sheets for myocardial infarction using a 3D-dynamic system.

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Cell sheet techniques offer a promising future for myocardial infarction (MI) therapy; however, insufficient nutrition supply remains the major limitation in maintaining stem cell bioactivity in vitro. In order to enhance cell sheet mechanical strength and bioactivity, a decellularized porcine

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